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classificationCPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-5094
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-5088
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-502
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-5008
classificationIPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/G01N33-50
filingDate 1999-05-03-04:00^^<http://www.w3.org/2001/XMLSchema#date>
grantDate 2000-02-08-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_2a2e945ee6b8b3f71103d7b2c3f5d967
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_10ac6b7acf990633a9bed8461f3b58c0
publicationDate 2000-02-08-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-6022699-A
titleOfInvention Myeloperoxidase assay of endotoxin-induced inflammation
abstract An improved model of endotoxin-induced inflammation is obtained by eliminating the interference in the biochemical assay of myeloperoxidase caused by endogenous reductants and cellular constituents containing free thiol functional groups. The interference was eliminated by 1) extensively diluting soluble, interfering substances and 2) blocking tissue sulfhydril functional groups during tissue homogenization. The improved model can be used to assess the therapeutic potential of anti-inflammatory agents. For example, the model can be used to evaluate topically administrable ophthalmic anti-inflammatory agents in Lewis rats.
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priorityDate 1999-05-03-04:00^^<http://www.w3.org/2001/XMLSchema#date>
type http://data.epo.org/linked-data/def/patent/Publication

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